P3C380: Smitten by a Kitten: An Unusual Cause of Leg Weakness in a Pediatric Patient

Introduction: Cat Scratch Disease, caused by gram-negative bacillus Bartonella henslae, is characterized by regional lymphadenopathy and less commonly, ocular and neurological manifestations. Anti-myelin oligodendrocyte glycoprotein-associated disease (MOGAD) is a condition in which IgG antibodies bind myelin oligodendrocyte glycoprotein (MOG), resulting in demyelination. Anti-MOG antibodies in pediatric patients may cause acute disseminated encephalomyelitis (ADEM), non-ADEM encephalitis, transverse myelitis, and neuromyelitis optica spectrum disorder. The following demonstrates the first reported case of suspected Bartonella-associated MOGAD in a pediatric patient.

Case Description: A previously healthy 9-year-old male presented with one day of lower back pain, bilateral leg weakness, feet tingling, and nocturnal enuresis. He also reported two weeks of right axillary lymphadenopathy. Physical exam demonstrated decreased strength, hyporeflexia, and decreased range of motion of bilateral lower extremities resulting in an inability to ambulate. He had one palpable, enlarged, tender right axillary lymph node and one left inguinal enlarged lymph node. Superficial, linear abrasions were present on his bilateral upper arms and legs, which were attributed to scratches from a new kitten.

Total spine MRIs demonstrated abnormal T2 hyperintensities throughout the spinal cord from C2 to the conus medullaris without enhancement. Brain MRI showed patchy T2 intensities throughout the cerebral subcortical and deep white matter, cerebral cortex, thalami, caudate heads, right cerebellar white matter, and upper medulla without enhancement. Diagnostic testing included an infectious workup with serum and cerebrospinal fluid studies including a CNS demyelinating panel. An autoimmune workup was performed with negative ANA, RF, and ANCA. The patient received empiric IV methylprednisolone for five days and IVIG for three days. He had resolution of bilateral lower extremity weakness and paresthesias, no further episodes of incontinence, and no new neurologic symptoms. He was discharged with an oral steroid taper. Subsequently, Bartonella henselae titer and anti-MOG antibodies resulted positive. Given these findings, the final leading diagnosis was MOGAD related to Bartonella infection.

Discussion: The differential diagnosis of this patient’s myelitis included autoimmune (MOGAD, ADEM), post-infectious etiologies, and paraneoplastic processes. Although rare in children, one-third of pediatric acute demyelinating syndrome (ADS) initial cases are associated with Anti-MOG antibodies. Bartonella is most often transmitted from kittens or cats to children 5 to 9 years old through contact via scratching, licking, or biting, leading to regional lymphadenopathy near the site of inoculation. There have been reports of Bartonella-associated transverse myelitis, Guillain-Barre Syndrome, encephalopathy, and autoimmune thyroiditis. However, no previous reports of Bartonella-associated MOGAD in the pediatric population exist in the literature.

Conclusion: This is the first report of MOGAD associated with Bartonella infection demonstrating possible secondary immune-mediated complications of Bartonella in the pediatric population. For children presenting with symptoms of ADS, testing and treatment for Bartonella Henslae infection should be considered among patients with a history of contact with kittens or cats.